L3 Somatosensation/Pain Flashcards
Sensory transduction
process of converting energy of a stimulus into an electrical signal
similar in all somatosensory afferents
stimulus alters the permeability of cation channels in afferent nerve, creating a receptor potential
Type of neurons in somatosensory system
pseudounipolar
reside in the dorsal root ganglion
allows for the electrical activity to “skip” the cell body on its way to the target
receptor potential
depolarizing current in afferent nerve endings
has to be a high enough magnitude or have a strong enough stimulus to reach threshold
Free nerve endings
afferent fibers that lack specialized receptor cells have free nerve endings
especially important in pain
mechanoreceptors would be an example of a specialized receptor cell
Proprioception afferent nerve characteristics
Receptor type: muscle spindle
Axon type: Ia, II
Largest diameter, fastest speed
Touch afferent nerve characteristics
Receptors: merkel, meissner, pacinian, ruffini
Axon: A-Beta
smaller diameter and slower speed then proprioception
Pain/Temperature afferent nerve characteristics
Receptor: free nerve endings
Axon: A-delta
smaller diameter and slower speed then touch
Pain/Temp/Itch/Non-dscriminative touch afferent nerve characteristics
Receptor: free nerve endings, unmyelinated
Axon: C
smallest diameter, slowest speed
Merkel afferents
slow adapting, enriched in finger tips. Signal the tactic aspect of a touch stimulus, such as pressure
detailed, best for braille
Meissner afferents
rapidly adapting fibers that innervate skin more densely then Merkel. Large receptive fields, transmit signal with reduced spatial resolution
good at detecting relatively low-frequency vibrations that occur when textured objects are moved across the skin
detects slippage between skin an an object held in the hand
Pacinian afferents
rapidly adapting fibers
detect vibrations transmitted through objects that contact the hand or are being grasped in the hand
Ruffini afferents
slow adapting
responsive to skin stretches
Rapidly adapting afferents
fire rapidly when a stimulus is first presented, then fall silent in the presence of continued stimulation
effective in providing info about changes in ongoing stimulation
Pacinian & Meissner
Slowly adapting afferents
generate a more sustained discharge in the presence of ongoing stimulus
better suited to provide info about spatial attributes of the stimulus, like size and shape
Ruffini and Merkel
Proprioceptors
provide info about mechanical forces arising from within the body itself
examples include muscle spindles, golgi tendon organs, joint receptors
Muscle spindles
-found in majority of striated muscles
-consist of specialized intrafusal muscle fibers surrounded by a capsule of connective tissue
-arranged with extrafusal fibers of skeletal muscle
-when the muscle is stretched, the tension on the intrafusal fiber activates mechanically gated ion channels in nerve endings
Golgi tendon organs
-low-threshold mechanoreceptors in tendons that inform the CNS about changes in muscle tension
DCML Pathway
carries light touch and proprioception
1. information travels via dorsal root through gracile fasciculus or cuneate
2. Synapses on gracile nucleus
3. Decussates in the arcuate fibers
4. Travels up the medial leminscus
5. Synapses on the VPL
6. Travels through the internal capsule, corona radiata, to end at SI
Hierarchy of somatosensory cortex
S2 is dependent on the activity in S1
S2 sends info to limbic structures
S1 also sends info to Broadman areas of 5 and 7, which supply inputs to the frontal lobe. Help to integrate information from sensory to motor cortex
Nociceptors
initiate the sensation of pain
arise from cell bodies in dorsal root ganglia
end in free nerve endings
conduct slowly
usually lightly myelinated or unmyelinated
usually A delta or C group axons
First pain
sharp
A-delta fibers usually convey this feeling
Second pain
delayed, diffused, long lasting
C-fiber convey these
A-delta fibers
convey first pain
has two classes that respond to heat at different levels
Type 1 = dangerous heat, low mechanical
Type 2 = Low heat, high mechanical
C-fibers
most respond to all nociceptive stimuli, making them “polymodal”
Nociceptors vs Thermoceptors
Action potentials are fired at same rate at all temps at thermoreceptor
number and frequency of firing increase at nocicoceptors
Capsaicin
Found in peppers, activates responses in C fibers
the less TRPV1 receptors you have, the more spice you can handle
ALS Pathway
- Free nerve ending
- Lissauers Tract*
- Decussate in ventral commisure
- Synapses in Medulla, Pons on RF and Midbrain on PAG
- Remaining fibers travel up and synapse in thalamus on MD, VPL, VMP
- MD –> Cingulate gyrus, VPL –> SI, VMP –> insula
- some fibers travel up to raphe nuclei to then synapse on the PAG
Rexed’s laminae
descriptive divisions of spinal gray matter in cross section
process and transmit sensory info, coordinate motor functions
C fibers will terminate on Rex I/II
A delta will terminate on Rex I/V
I/V = brainstem and thalamic
Non-nocioceptive = III/IV/V
Wide dynamic range neurons
Multimodal lamina V neurons are known as this
some receive visceral sensory input as well as pain inputs
could be an explanation for referred pain
Spinal cord lesion
Unilateral spinal cord lesion
Loss of ALS (pain, temp, itch) on CONTRALATERAL side
Loss of DCML (sensation, touch, pressure, etc) on IPSILATERAL SIDE
this is because in the ALS the 2nd order neurons in I and V cross midline and ascend to brainstem vs DCML, they cross in medulla
Sensory discriminative pain
gives us location, intensity, quality of noxious stimuli
Depends on info relayed through the VPL to S1 and S2
ALS tract manages it
Affective-motivational pain
unpleasant feeling, fear, anxiety, fight or flight response
targets: reticular formation, PAG, superior colliculus, parabrachial nucleus
Parabrachial nucleus
processes and relays second pain to amygdala, hypothalamus, thalamic nuclei
help to elaborate affective-motivational aspects of pain
ALS and absence of DCML
ALS is capable of mediating something like nondiscriminative touch, but stereognosis is impaired and it lacks fine spatial resolution
C fibers do this
Other modalities of ALS
responsible for innocuous temperature sensation, which are mediated by fibers that don’t respond to noxious stimulus or mechanical stimulation, just change in temp
cells in lamina 1 cause the actions that relate to homeostasis
Hyperalgesia
following a painful stimulus that caused tissue damage
stimuli in area of injury are seen as significantly painful, when they should be slightly painful
Peripheral sensitization
results from interactions nociceptors with the inflammatory soup of substances released at tissue damage
heightened sensitivity of nerve endings and an increased responsiveness to pain signals
These substances/molecules cause the nerve endings to become sensitized, making them more likely to respond to low level stimuli
Purpose of peripheral sensitization
protecting the injured area
promote healing
guard against infection
Central Sensitization
rapid onset, activity-dependent increase in the excitability of neurons in the dorsal horn of the spinal cord
triggered by activity at nociceptors in dorsal horn
causes increase in pain and sensitivity in the CNS
causes subthreshold levels of activity to be sufficient to generate APs in dorsal horn neurons
What type of sensitization is the underlying process for developing chronic pain?
central
Allodynia
induction of pain by a normally non-painful stimulus
occurs immediately after painful event and can outlast the pain of the stimulus by several hours
What contributes to central sensitization?
Windup
progressive increase in the discharge rate of dorsal horn neurons in response to repeated low-frequency activation of nociceptive afferents.
EASIER: refers to an amplified and prolonged pain response in the spinal cord
lasts only during stimulation and happens b/c of summation of slow synaptic potentials
the delta stimulus remains strong because there is a increased sensitivity to glutamate
Neuropathic pain
when afferent nerve fibers or central pathways are damaged, sensitization can persist causing neuropathic pain
can arise without stimulus or can be produced by a mild stimulus
constant burning sensation that can have shooting, stabbing, or jolts
no inflammation process
Phantom limbs/pain
most common cause of chronic pain syndromes
possibly due to maladaptive plasticity in neural circuits
reorganization of mapping/neural plasticity, residual nerve activity, central sensitization can cause it
Pain modulation
- PAG–> can produce analgesia, inhibits nociceptive neurons in dorsal horn of SC
- Parabrachial nucleus, dorsal raphe, locus ceruleus, medullary RF –> release NTs that can excite or inhibit neurons
- Descending tracts–> excite or inhibit dorsal horn, impact efficacy of nociceptive transmission
- Interactions between mechanoreceptive afferents and neural circuits (rubbing toe after hitting it)
Gate theory of pain
flow of nociceptive info through the SC is modulated by activation of large myelinated fibers of low-threshold mechanoreceptors
Placebo effect
responses can be blocked by antagonist opioids (in the example of pain medication), there is a physiologic basis for pain relief experienced–pts pain is real
causes activation of endogenous opioid receptors, also can activate descending pathways which modulate pain
Endogenous Opioids
located in the PAG
three types: enkephalins, endorphins, dynorphins
areas of the nervous system that produce analgesics are very receptive to opioids, meaning there are opioid sensitive neurons
these substances reduce the level of activity passed onto higher processing centers
Endogenous cannabinoids
thought to decrease the release of neurotransmitters, so essentially modulating neuronal excitability
cannabinoids can block the electrical stimulation of the PAG, stopping pain signals from traveling elsewhere
noxious stimuli cause increased cannabinoids in PAG
PAG roles in Pain
- pain inhibition, causes release of opioids
- Descending tract modulation
- Modulates emotional response to pain
- Placebo effect
- Integrates sensory and emotional information to modulate pain
